ArticleOncology letters2017
Common mechanism of pathogenesis in various types of metastatic osteosarcoma.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Targeting ferroptosis in osteosarcoma.Journal of bone oncology · 2021Review
- Long noncoding RNA KCNQ1 opposite strand/antisense transcript 1 promotes osteosarcoma progression through miR-154-3p/KLF12.American journal of translational research · 2021Article
- Identification of potential diagnostic and therapeutic target genes for lung squamous cell carcinoma.Oncology letters · 2019Article
- miR-210 promotes human osteosarcoma cell migration and invasion by targeting FGFRL1.Oncology letters · 2018Article
- Hedgehog signalling in the tumourigenesis and metastasis of osteosarcoma, and its potential value in the clinical therapy of osteosarcoma.Cell death & disease · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the common metastatic mechanism in various types of metastatic osteosarcoma (OS). Gene expression profiles generated from the metastatic OS KHOS and KRIB cell lines and the non-metastatic OS HOS cell line were compared. Two groups of differentially expressed genes (DEGs) between KHOS or KRIB and HOS were screened (P<0.01 and |fold change| ≥2) and then underwent Gene Ontology (GO) and pathway enrichment analyses. Subsequently, the protein-protein interaction (PPI) network was constructed and the subnetwork was mined. Furthermore, overlapping DEGs of these two groups were identified and pathway enrichment and regulatory network analyses were performed. A total of 1,552 and 1,330 DEGs from KHOS vs. HOS and KRIB vs. HOS were obtained, respectively. GO and pathway enrichment analyses of DEGs between KRIB and HOS, including anatomical structure morphogenesis and focal adhesion, were similar to those between KHOS and HOS. Vascular endothelial growth factor A and epidermal growth factor receptor were hub nodes in the PPI network for KHOS and KRIB. Subnetworks of these two groups were similar. In addition, 421 upregulated and 595 downregulated overlapping genes were enriched in the mitogen-activated protein kinase and transforming growth factor-β signaling pathways. Furthermore, seven vital transcription factors, including hes-related family bHLH transcription factor with YRPW motif 1 (HEY1), were obtained. Overall, different types of metastatic OS were shown to exhibit a similar mechanism of pathogenesis. With the exception of cell adhesion and angiogenesis, recapitulation of the morphogenetic processes facilitates OS tumor formation and metastasis. Genes such as HEY1 are important for metastatic OS. Further studies are required in order to confirm these results.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.